Curare and low blood pressure effects on direct cortical responses

The hypothesis that d-tubocurarine injected intravenously blocks synaptic transmission by a direct action in the cerebral cortex was examined. Injections of 3 mg/kg d-tubocurarine caused either no fall, moderate decreases, or complete obliteration of direct cortical responses (DCR's) with little return to control levels within 30–60 minutes. Blood pressure was recorded and drops to 50–60 mm Hg or below were associated with moderate to severe decreases of DCR's; drops below 40 mm Hg with elimination of the DCR. Diminishing the blood pressure to 50–60 mm Hg by bleeding resulted in moderately to greatly decreased DCR's. Bleedings to a pressure of 35–40 mm Hg might give rise to an ‘enhancing effect’ before DCR's were completely diminished. During enhancement DCR's became several times larger than control height. This effect was interpreted as a differential loss of an inhibitory component. Decrease of DCR's after injecting d-tubocurarine is considered secondary to the lower blood pressure.

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Evaluating the use of a lower blood pressure target to guide drug treatment in critically ill children with low blood pressure

http://isrctn.com/ ◽

10.1186/isrctn20609635 ◽

2021 ◽

Author(s):

David Inwald

Keyword(s):

Blood Pressure ◽

Drug Treatment ◽

Critically Ill ◽

Critically Ill Children ◽

Blood Pressure Target ◽

Lower Blood Pressure ◽

Lower Blood ◽

Low Blood Pressure

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Catecholamines in Turkeys with High or Low Blood Pressure: Effects of Tyrosine Hydroxylase Inhibitor and Ganglionic Blocker

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y72-101 ◽

1972 ◽

Vol 50 (7) ◽

pp. 697-702 ◽

Cited By ~ 6

Author(s):

M. E. El-Halawani ◽

P. E. Waibel ◽

R. Appel ◽

A. L. Good ◽

G. E. Duke

Keyword(s):

Blood Pressure ◽

Tyrosine Hydroxylase ◽

Left Ventricle ◽

Genetic Selection ◽

Pressure Effects ◽

Norepinephrine Release ◽

Low Blood Pressure ◽

Blood Pressure Effects ◽

Selection For

Following six generations of genetic selection for hyper- or hypotensive turkeys, tissues were assayed for catecholamines. The concentrations of norepinephrine and epinephrine were essentially the same in both groups except for the posterior aorta and the left ventricle. The latter tissues showed higher concentration of norepinephrine in the hypertensive birds.The administration of α-methyl-L-tyrosine or mecamylamine reduced norepinephrine to a greater extent in hyper- than in hypotensive turkeys. The results suggest that hypertension may be caused by increased rate of norepinephrine release.

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Reduction in Pain Sensitivity from Pharmacological Elevation of Blood Pressure in Persons with Chronically Low Blood Pressure

Journal of Psychophysiology ◽

10.1027/0269-8803.23.3.104 ◽

2009 ◽

Vol 23 (3) ◽

pp. 104-112 ◽

Cited By ~ 12

Author(s):

Stefan Duschek ◽

Heike Heiss ◽

Boriana Buechner ◽

Rainer Schandry

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Pain Sensitivity ◽

Pain Threshold ◽

Pain Perception ◽

Drug Effects ◽

Pressure Effects ◽

Double Blind ◽

Low Blood Pressure ◽

Present Trial

Recent studies have revealed evidence for increased pain sensitivity in individuals with chronically low blood pressure. The present trial explored whether pain sensitivity can be reduced by pharmacological elevation of blood pressure. Effects of the sympathomimetic midodrine on threshold and tolerance to heat pain were examined in 52 hypotensive persons (mean blood pressure 96/61 mmHg) based on a randomized, placebo-controlled, double-blind design. Heat stimuli were applied to the forearm via a contact thermode. Confounding of drug effects on pain perception with changes in skin temperature, temperature sensitivity, and mood were statistically controlled for. Compared to placebo, higher pain threshold and tolerance, increased blood pressure, as well as reduced heart rate were observed under the sympathomimetic condition. Increases in systolic blood pressure between points of measurement correlated positively with increases in pain threshold and tolerance, and decreases in heart rate were associated with increases in pain threshold. The findings underline the causal role of hypotension in the augmented pain sensitivity related to this condition. Pain reduction as a function of heart rate decrease suggests involvement of a baroreceptor-related mechanism in the pain attrition. The increased proneness of persons with chronic hypotension toward clinical pain is discussed.

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